The biophysical element, antithrombin, which inhibits thrombin action, theoretically exists in several types, such as, I, II, III, etc. However, only antithrombin III has been proved to actually exist. That is, it is synthesized in the human liver, exists in the human blood, and controls the coagulation system. It has also been proved that antithrombin III inhibits thrombin action more quickly in the presence of heparin. In other words, heparin itself does not cause anticoagulation, but it promotes the action of antithrombin III for immediate anticoagulation.
Antithrombin III is one of the major regulators of enzymes generated during the activation of the coagulation system. For this reason, antithrombin levels are expected to decrease in patients with a substantial activation of their coagulation system. This should occur when the rate of antithrombin III consumption exceeds its rate of production by the liver hepatocyte. This has been documented by a number of investigators who measured antithrombin III levels in clinical conditions that are associated with disseminated intravascular coagulation (D.I.C.) and several other conditions including malignancies, acute promyelocytic leukemias, severe burns with infections, sepsis and preeclampsia.
In order to provide proper treatment for D.I.C. in the past, heparin was mainly administered therewith. However, it has already been shown that heparin does not work effectively when antithrombin III is decreased in the blood. Accordingly, it has been recommended to administer dried concentrated human antithrombin III, so that the lack of antithrombin III can be corrected.
With regard to the effect of dried concentrated antithrombin III, no report has been issued, wherein the clinical use of antithrombin III in ophthalmology has been suggested.
More particularly, a patient's visual acuity is effected by fibrin deposits that form on an intraocular lens surface a few days after the intraocular lens has been implanted in a cataract patient.
To prevent fibrin accumulations, many surgeons have prescribed anti-inflammatory drugs such as Indomethacin or Corticosteriods. Unfortunately these drugs may produce significant harmful side effects.
Such fibrin deposits on the implanted intraocular lens surface is a problem which must be resolved because obstruction of the patient's vision or postoperative posterior synechia may result.
As previously mentioned, anti-inflammatory drugs are used to treat this condition, but the administration of Indomethacin or Corticosteroids is associated with a delay in wound healing according to reliable medical/clinical reports recently.
Fibrin formation in the ocular chamber is regarded as a formation occurring on the outside of blood vessels, and fibrin clot formation on the intraocular lens is regarded as iridocyclitis caused by fibrin deposition.
When the blood aqueous barrier is broke, the aqueous humor becomes similar to blood plasma and is confronted with corneal endothelial cells which look quite similar to blood endothelial cells, both in style and function. The ocular chamber, which is inherently not a blood vessel, becomes similar to a blood vessel for the time being.
On checking the movement of tissue plasminogen activator after cataract surgery or intraocular lens implant surgery, the degree to which the blood aqueous barrier breaks reaches the maximum after said surgery (after 1 or 2 days), and it recovers gradually after a period of time. However, the activation value of tissue plasminogen activator shows a two-phase deterioration, such that some deterioration is seen on the first day after the surgery, while rapid and conspicuous recovery is seen on the second day. This type of deterioration is evidence of the transient situation of the corneal endothelial cell function, and the recovery is evidence of the reaction of the cells' function against fibrinolytic action for coagulation in the aqueous humor.
Fibrin formation on an implanted intraocular lens, that occurs on the fourth to seventh postoperative days, is noticed with the activation of the intrinsic pathway of the blood coagulation system on the polymethylmethacrylate surface in the fibrinogen-rich aqueous humor. Consequently, the imbalance between coagulation and the fibrinolytic system in the aqueous humor may result in the fibrin formation on the implanted intraocular lens.